ArticleTranslational neurodegeneration2026
Calbindin-D28k deficiency mediates tau-driven hippocampal hyperexcitement and cognitive impairment.
Article in Translational neurodegeneration, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMedial temporal lobe hyperexcitation or seizures originating from the hippocampus are frequently observed in Alzheimer's disease (AD) patients, contributing to accelerated cognitive decline. As the hippocampus is an early vulnerable area of tau pathology, the mechanisms by which abnormal tau aggregation promotes temporal lobe epilepsy (TLE) remain poorly understood.
methodsWe investigated the role of AD-like hippocampal tau aggregation in neuronal hyperexcitation using transgenic (Tg) tau-driven mice. Effects of tau aggregation on intracellular calcium dynamics were assessed by calcium imaging. Neuronal/network hyperexcitability and seizure susceptibility were evaluated through patch-clamp electrophysiology,
resultsTau accumulation in the hippocampal CA1/DG CaMKII-positive excitatory neurons reduced CB expression with disruption of calcium homeostasis. This dysregulation increased neuronal excitability, diminished synaptic protein levels, and increased seizure susceptibility and cognitive impairment. AAV-driven CB restoration in CA1/DG neurons attenuated both hyperexcitability and cognitive deficits. In the brains of AD patients, reduced CB expression was associated with cognitive deterioration and advanced disease stages.
conclusionsTau aggregation drives calcium dysregulation and hippocampal neuronal hyperexcitation through reducing CB expression. These results establish a potential mechanistic link between tauopathy and TLE pathogenesis in AD, providing evidence for CB as a promising therapeutic target for mitigating seizure risk and related cognitive decline in AD.
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